| Project/Area Number |
23659666
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Thoracic surgery
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| Research Institution | Kyoto University |
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Principal Investigator |
DATE Horoshi 京都大学, 医学(系)研究科(研究院), 教授 (60252962)
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| Co-Investigator(Kenkyū-buntansha) |
黄 政龍 公益財団法人田附興風会医学研究所 (10271511)
園部 誠 京都大学, 医学(系)研究科 (00432378)
毛受 暁史 京都大学, 医学(系)研究科 (30527081)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | FGFR / ｓｈRNA / アデノウィルス / ベクター / 遺伝子治療 / shRNA / ＦＧＦＲ / ｓｈＲＮＡ / sh RNA |
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| Research Abstract |
We performed an experimental study on the gene therapy using a FGFR-inhibiting vector for a new treatment against lung squamous cell carcinomas. First, we have done a clinical study on the inntratumoral expressions of FGFR family genes. Consequently, we considered that not only FGFR1 but also FGR2 could be target genes for treatments. We produced a FGFR2-inhibiting vector using an adenoviral vector (Ad-shFGFR2). in vitro experiments using the Ad-shFGFR2 were performed against a lung cancer cell line A549, which has high expression levels of FGFR2. The Ad-shFGFR2 effectively knocked down the FGFR2 expression (approximately 85%). However, MTT assays revealed that the Ad-shFRFR2 did not effectively inhibit the growth of tumor cells. Therefore, considering that FGFR2 may not be a simple driver gene, we perform an experimental study using co-transfection with other candidates of driver genes.
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